scholarly journals Bacterial Exposure Induces and Activates Matrilysin in Mucosal Epithelial Cells

2000 ◽  
Vol 148 (6) ◽  
pp. 1305-1315 ◽  
Author(s):  
Yolanda S. López-Boado ◽  
Carole L. Wilson ◽  
Lora V. Hooper ◽  
Jeffrey I. Gordon ◽  
Scott J. Hultgren ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Acute Infection ◽  
Human Colon ◽  
Cell Types ◽  
The Body ◽  
Apical Surface ◽  
Tracheal Epithelial Cells ◽  
Lung Carcinoma Cells ◽  
Tracheal Epithelial ◽  
And Function

Matrilysin, a matrix metalloproteinase, is expressed and secreted lumenally by intact mucosal and glandular epithelia throughout the body, suggesting that its regulation and function are shared among tissues. Because matrilysin is produced in Paneth cells of the murine small intestine, where it participates in innate host defense by activation of prodefensins, we speculated that its expression would be influenced by bacterial exposure. Indeed, acute infection (10–90 min) of human colon, bladder, and lung carcinoma cells, primary human tracheal epithelial cells, and human tracheal explants with type 1–piliated Escherichia coli mediated a marked (25–50-fold) and sustained (>24 h) induction of matrilysin production. In addition, bacterial infection resulted in activation of the zymogen form of the enzyme, which was selectively released at the apical surface. Induction of matrilysin was mediated by a soluble, non-LPS bacterial factor and correlated with the release of defensin-like bacteriocidal activity. Bacteria did not induce matrilysin in other cell types, and expression of other metalloproteinases by epithelial cells was not affected by bacteria. Matrilysin was not detected in germ-free mice, but the enzyme was induced after colonization with Bacteroides thetaiotaomicron. These findings indicate that bacterial exposure is a potent and physiologically relevant signal regulating matrilysin expression in epithelial cells.

Molecular responses of rat tracheal epithelial cells to transmembrane pressure

2000 ◽  
Vol 278 (6) ◽  
pp. L1264-L1272 ◽  
Author(s):  
Barbara Ressler ◽  
Richard T. Lee ◽  
Scott H. Randell ◽  
Jeffrey M. Drazen ◽  
Roger D. Kamm
Keyword(s):  
Smooth Muscle ◽  
Epithelial Cells ◽  
Muscle Activation ◽  
Primary Cultures ◽  
Transmembrane Pressure ◽  
Apical Surface ◽  
Dependent Manner ◽  
Tracheal Epithelial Cells ◽  
Compressive Stresses ◽  
Tracheal Epithelial

Smooth muscle constriction in asthma causes the airway to buckle into a rosette pattern, folding the epithelium into deep crevasses. The epithelial cells in these folds are pushed up against each other and thereby experience compressive stresses. To study the epithelial cell response to compressive stress, we subjected primary cultures of rat tracheal epithelial cells to constant elevated pressures on their apical surface (i.e., a transmembrane pressure) and examined changes in the expression of genes that are important for extracellular matrix production and maintenance of smooth muscle activation. Northern blot analysis of RNA extracted from cells subjected to transmembrane pressure showed induction of early growth response-1 (Egr-1), endothelin-1, and transforming growth factor-β1 in a pressure-dependent and time-dependent manner. Increases in Egr-1 protein were detected by immunohistochemistry. Our results demonstrate that airway epithelial cells respond rapidly to compressive stresses. Potential transduction mechanisms of transmembrane pressure were also investigated.

Differential regulation of centrin genes during ciliogenesis in human tracheal epithelial cells

1998 ◽  
Vol 275 (6) ◽  
pp. L1145-L1156 ◽  
Author(s):  
Michel LeDizet ◽  
James C. Beck ◽  
Walter E. Finkbeiner
Keyword(s):  
Epithelial Cells ◽  
Calcium Binding ◽  
Cell Types ◽  
Differential Regulation ◽  
Pcr Analysis ◽  
Rt Pcr ◽  
Tracheal Epithelial Cells ◽  
Tracheal Epithelial ◽  
Air Liquid Interface

Centrins are small calcium-binding proteins found in a variety of cell types, often in association with microtubule-organizing centers. Here we present results regarding the expression of centrins during the in vitro differentiation of human tracheal epithelial cells. When grown at an air-liquid interface, these cells differentiate into mucus-secreting cells or undergo ciliogenesis. In immunofluorescence and immunoelectron microscopy experiments, an anti-centrin antibody stained exclusively the basal bodies of the ciliated cells. There was no staining over the axonemes or the striated rootlets. Northern blots and RT-PCR analysis of the three known human centrin genes showed that these genes have distinct patterns of expression during the growth and differentiation of human tracheal epithelial cells. Centrin-1 is never transcribed. Centrin-2 mRNA is present at all times, and its concentration increases when ciliogenesis occurs. Centrin-3 mRNA is found at a constant level throughout the entire process. This differential regulation suggests that centrins are not interchangeable but instead have unique functions.

A subset of mouse tracheal epithelial basal cells generates large colonies in vitro

2004 ◽  
Vol 286 (4) ◽  
pp. L631-L642 ◽  
Author(s):  
Kelly G. Schoch ◽  
Adriana Lori ◽  
Kimberlie A. Burns ◽  
Tracy Eldred ◽  
John C. Olsen ◽  
...  
Keyword(s):  
Stem Cells ◽  
Epithelial Cells ◽  
The Body ◽  
Growth Potential ◽  
Small Subset ◽  
Basal Cells ◽  
Airway Epithelial ◽  
Epithelial Stem Cells ◽  
Tracheal Epithelial Cells ◽  
Tracheal Epithelial

Airway epithelial stem cells are not well characterized. To examine clonal growth potential, we diluted single, viable B6.129S7-Gtrosa26 (Rosa26) mouse tracheal epithelial cells that constitutively express β-galactosidase into non-Rosa26 cells in an air-liquid interface cell culture model; 1.7% of the cells formed colonies of varying size, and, on average, 0.1% of the cells formed large colonies. Thus only a small subset of cells displayed progenitorial capacity suggestive of stem or early transient amplifying cells. Prior studies identified cells with high keratin 5 (K5) promoter activity in specific niches in the mouse trachea and these cells corresponded to the location of bromodeoxyuridine label-retaining cells, thought to be stem cells (Borthwick DW, Shahbazian M, Todd KQ, Dorin JR, and Randell SH, Am J Respir Cell Mol Biol: 24: 662–670, 2001). To explore the hypothesis that stem cells were present in the K5-expressing compartment, we created transgenic mice in which enhanced green fluorescent protein (EGFP) was driven by the K5 promoter. These mice expressed EGFP in most basal cells of the body including a subset of tracheal basal cells apparently located in positions similar to previously identified stem cell niches. Flow cytometrically purified EGFP-positive cells had an overall colony-forming efficiency 4.5-fold greater than EGFP-negative cells, but the ability to generate large colonies was 12-fold greater. Thus adult mouse tracheal epithelial cells with progenitorial capacity sufficient to generate large colonies reside in the basal cell compartment. These studies are a first step toward purification and characterization of airway epithelial stem cells.

scholarly journals West Nile Virus Capsid Degradation of Claudin Proteins Disrupts Epithelial Barrier Function

2009 ◽  
Vol 83 (12) ◽  
pp. 6125-6134 ◽  
Author(s):  
Guruprasad R. Medigeshi ◽  
Alec J. Hirsch ◽  
James D. Brien ◽  
Jennifer L. Uhrlaub ◽  
Peter W. Mason ◽  
...  
Keyword(s):  
West Nile Virus ◽  
Epithelial Cells ◽  
Acute Infection ◽  
Cell Types ◽  
Epithelial Barrier ◽  
West Nile ◽  
Epithelial Barrier Function ◽  
Barrier Formation ◽  
Lysosomal Proteases ◽  
And Function

ABSTRACT During acute infection, West Nile virus (WNV) has been reported to infect a variety of cell types in various tissues of both experimentally and naturally infected hosts. Virus infects epithelial cells in the skin, kidney, intestine, and testes, although the importance of these findings is unclear. In the current study, we have observed that WNV infection of kidney tubules in mice coincides with the loss of expression of several members of the claudin family. Proteins of this family are often involved in epithelial barrier formation and function. WNV infection of epithelial cells in culture resulted in a decrease in the transepithelial electrical resistance, an increase in the efflux of mannitol across the monolayer, and a loss of intracellular levels of claudin-1 to -4. WNV capsid alone was sufficient for the degradation event, which was mediated through lysosomal proteases. Since epithelial cells are frequent sites of WNV infection, these observations imply a potential mechanism for virus dissemination and extraneural pathogenesis.

Endothelin stimulates chloride secretion across canine tracheal epithelium

1991 ◽  
Vol 261 (2) ◽  
pp. L188-L194 ◽  
Author(s):  
P. I. Plews ◽  
Z. A. Abdel-Malek ◽  
C. A. Doupnik ◽  
G. D. Leikauf
Keyword(s):  
Epithelial Cells ◽  
Short Circuit ◽  
Second Messengers ◽  
Short Circuit Current ◽  
Chloride Secretion ◽  
Tracheal Epithelium ◽  
Membrane Phospholipids ◽  
Cl Secretion ◽  
Tracheal Epithelial Cells ◽  
Tracheal Epithelial

The endothelins (ET) are a group of isopeptides produced by a number of cells, including canine tracheal epithelial cells. Because these compounds are endogenous peptides that may activate eicosanoid metabolism, we investigated the effects of ET on Cl secretion in canine tracheal epithelium. Endothelin 1 (ET-1) was found to produce a dose-dependent change in short-circuit current (Isc) that increased slowly and reached a maximal value within 10-15 min. When isopeptides of ET were compared, 300 nM ET-1 and ET-2 produced comparable maximal increases in Isc, whereas ET-3 produced smaller changes in Isc (half-maximal concentrations of 2.2, 7.2, and 10.4 nM, respectively). Ionic substitution of Cl with nontransported anions, iodide and gluconate, reduced ET-1-induced changes in Isc. Furthermore, the response was inhibited by the NaCl cotransport inhibitor, furosemide. In paired tissues, ET-1 significantly increased mucosal net 36Cl flux without significant effect on 22Na flux. The increase in Isc induced by ET was diminished by pretreatment with indomethacin. The second messengers mediating the increase in Isc were investigated in cultured canine tracheal epithelial cells. ET-1 stimulated the release of [3H]arachidonate from membrane phospholipids, increased intracellular Ca2+ (occasionally producing oscillations), and increased adenosine 3',5'-cyclic monophosphate accumulation. The latter was diminished by indomethacin. Thus ET is a potent agonist of Cl secretion (with the isopeptides having the following potency: ET-1 greater than or equal to ET-2 greater than ET-3) and acts, in part, through a cyclooxygenase-dependent mechanism.

scholarly journals Fucoxanthin Ameliorates Oxidative Stress and Airway Inflammation in Tracheal Epithelial Cells and Asthmatic Mice

Cells ◽  
2021 ◽  
Vol 10 (6) ◽  
pp. 1311
Author(s):  
Shu-Ju Wu ◽  
Chian-Jiun Liou ◽  
Ya-Ling Chen ◽  
Shu-Chen Cheng ◽  
Wen-Chung Huang
Keyword(s):  
Oxidative Stress ◽  
Epithelial Cells ◽  
Airway Inflammation ◽  
Inflammatory Cytokines ◽  
Inflammatory Responses ◽  
Therapeutic Potential ◽  
Eosinophil Infiltration ◽  
Tracheal Epithelial Cells ◽  
Tracheal Epithelial ◽  
And Oxidative Stress

Fucoxanthin is isolated from brown algae and was previously reported to have multiple pharmacological effects, including anti-tumor and anti-obesity effects in mice. Fucoxanthin also decreases the levels of inflammatory cytokines in the bronchoalveolar lavage fluid (BALF) of asthmatic mice. The purpose of the present study was to investigate the effects of fucoxanthin on the oxidative and inflammatory responses in inflammatory human tracheal epithelial BEAS-2B cells and attenuated airway hyperresponsiveness (AHR), airway inflammation, and oxidative stress in asthmatic mice. Fucoxanthin significantly decreased monocyte cell adherence to BEAS-2B cells. In addition, fucoxanthin inhibited the production of pro-inflammatory cytokines, eotaxin, and reactive oxygen species in BEAS-2B cells. Ovalbumin (OVA)-sensitized mice were treated by intraperitoneal injections of fucoxanthin (10 mg/kg or 30 mg/kg), which significantly alleviated AHR, goblet cell hyperplasia and eosinophil infiltration in the lungs, and decreased Th2 cytokine production in the BALF. Furthermore, fucoxanthin significantly increased glutathione and superoxide dismutase levels and reduced malondialdehyde (MDA) levels in the lungs of asthmatic mice. These data demonstrate that fucoxanthin attenuates inflammation and oxidative stress in inflammatory tracheal epithelial cells and improves the pathological changes related to asthma in mice. Thus, fucoxanthin has therapeutic potential for improving asthma.

scholarly journals In Vitro Radiation-induced Effects on Rat Tracheal Epithelial Cells

2002 ◽  
Vol 43 (1) ◽  
pp. 27-27 ◽  
Author(s):  
CAROLE KUGEL ◽  
ISABELLE BAILLY ◽  
FRANÇOISE TOURDES ◽  
JEAN-LUC PONCY
Keyword(s):  
Epithelial Cells ◽  
Tracheal Epithelial Cells ◽  
Radiation Induced ◽  
Tracheal Epithelial
Sign in / Sign up

Export Citation Format

Share Document